This project continues a program of research that aims to document the patterns of risk and coping in children at high risk for the later development of alcoholism, alcohol abuse, and other drug problems as they move through early and middle childhood, and as they enter adolescence. Within the context of a broadly defined, biopsychosocial framework of inquiry, it will continue to describe those individual and contextual processes and structures that may lead either to developmental insult and heightened risk for later alcohol related difficulty, or to patterns of adaptation that appear likely to avoid or protect against it. The project is monitoring these processes at three year intervals, in a population based sample initially composed of 180 families, all of whom had a 3 to 5 year old son, and half of whom had at least one parent who was alcoholic, although frequently not formally diagnosed and not in treatment; the other half were drawn from the same neighborhoods as the alcoholic families, but neither parent had a history of significant alcohol or drug involvement. The work will track outcomes among the children and their parents at Wave 2, when the children are aged 6-8, at Wave 3 (children aged 9-11), and also begin Wave 4 (children aged 12-14). Two areas are to be given greater attention by way of design additions: (1) variations in child risk related to parental differences in alcoholic subtype (high vs. low antisocial) will be able to be more clearly identified by the addition of a subset of community families (N = 60), whose fathers are alcoholic but have had low levels of antisocial history; (2) by adding a parallel assessment protocol on daughters in all the families, the impact of parental alcoholism on female patterns of development, pertaining to both alcohol specific and nonspecific risk, will also be able to be evaluated. A number of hypotheses that have already received cross-sectional support will continue to guide the analyses: Children in higher risk families will have higher levels of aggressiveness, will show earlier evidence of negative mood, more problematic social relationships within and external to the family, greater deficits in cognitive functioning, more and more precocious acquisition of cognitive schemas about alcohol. Negative parent characteristics in the above areas are hypothesized to potentiate the child risk factors; positive parent characteristics (positive mood, cognitive competence, longer periods of either sobriety or nonproblem alcohol use) are hypothesized to dilute their development. Family load for alcoholism, as related to the subtype of greater parental antisociality, is hypothesized to mediate these effects. Non alcohol specific variables pertaining to parental comorbidity to achieved family social status, and to marital discord, are anticipated to moderate these relationships. Both path and structural equation models are to be utilized in mapping developmental variation.